PRKAR2B plays an oncogenic role in the castration-resistant prostate cancer
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Jianjun Sha1,2,*, Wei Xue1,*, Baijun Dong1, Jiahua Pan1, Xiaorong WU1, Dong Li1, Dongming Liu1, Yiran Huang1,2
1Department of Urology, Ren Ji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China
2School of Biomedical Engineering, Shanghai Jiaotong University, Shanghai, People’s Republic of China
Yiran Huang, email: firstname.lastname@example.org
Keywords: PRKAR2B, castration resistant, prostate cancer, CRPC, cell cycle
Received: July 11, 2016 Accepted: December 13, 2016 Published: December 20, 2016
Castration-resistant prostate cancer (CRPC) is an advanced form of prostate cancer. Despite some progresses have been made, the mechanism of CRPC development is still largely unknown, including the genes involved in its development have not been well defined. Here, we identifiedPRKAR2B to be a gene over-expressingin castration-resistant prostate cancer by analyzing the different online databases. Followed functional validation experiments showed that PRKAR2B promoted CRPC cell proliferation and invasion, and inhibited CRPC cell apoptosis. Whole genome transcriptome and GO enrichment analyses of the knock-down of PRKAR2B in CRPC cells showed that PRKAR2B mainly accelerated cell cycle biological process and modulated multiple cell cycle genes, such as CCNB1, MCM2, PLK1 and AURKB. Our study firstly identified PRKAR2B as a novel oncogenic gene involved in CRPC development and suggested it is a promising target for the future investigation and the treatment of CRPC.
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